miR-186 suppressed CYLD expression and promoted cell proliferation in human melanoma

被引:22
|
作者
Qiu, Haijiang [1 ]
Yuan, Suirong [1 ]
Lu, Xiaohe [2 ]
机构
[1] Guangzhou Med Univ, Guangzhou Peoples Hosp 1, Dept Ophthalmol, 1 Panfu Rd, Guangzhou 510180, Guangdong, Peoples R China
[2] Southern Med Univ, Zhujiang Hosp, Dept Ophthalmol, Guangzhou 510515, Guangdong, Peoples R China
关键词
miR-186; melanoma; CYLD; cell proliferation; DOWN-REGULATION; CANCER CELLS; MICRORNAS; GROWTH; DEUBIQUITINATION; SURVIVAL; PROTEIN; GLIOMA;
D O I
10.3892/ol.2016.5002
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Previous studies have shown that microRNA-186 (miR-186) is overexpressed in various human cancers and is associated with the regulation of the carcinogenic processes. However, the underlying mechanisms of this microRNA in melanoma remain largely unknown. In the present study, the overexpression of miR-186 was identified in melanoma tissues and melanoma cells compared to the expression of miR-186 in the matched tumor adjacent tissues and normal human epidermal melanocytes. Overexpression of miR-186 promoted the proliferation and anchorage-independent growth of melanoma cells, whereas inhibition of miR-186 reduced this effect. Bioinformatics analysis also revealed cylindromatosis (CYLD), a putative tumor suppressor, to be a potential target of miR-186. Luciferase reporter assays showed that miR-186 directly targeted the 3-untranslated regions of CYLD messenger RNA. Additional experiments showed that overexpression of miR-186 promoted the proliferation of melanoma cells, which was consistent with the inhibitory effects induced by knockdown of CYLD. In summary, the present study indicated that miRNA-186 plays a crucial role in melanoma growth and its oncogenic effect is mediated chiefly through the direct suppression of CYLD expression.
引用
收藏
页码:2301 / 2306
页数:6
相关论文
共 50 条
  • [1] MiR-767 promoted cell proliferation in human melanoma by suppressing CYLD expression
    Zhang, Kejin
    Guo, Ling
    GENE, 2018, 641 : 272 - 278
  • [2] MiR-186 inhibits cell proliferation and invasion in human cutaneous malignant melanoma
    Su, Bei-bei
    Zhou, Shu-wei
    Gan, Cai-bin
    Zhang, Xiao-ning
    JOURNAL OF CANCER RESEARCH AND THERAPEUTICS, 2018, 14 : S60 - S64
  • [3] miR-186 Inhibition Alters Cell Proliferation and Colony Formation in Prostate Cancer
    Jones, Dominique
    Hobbing, Katharine
    Schmidt, M.
    Clark, Geoffrey
    Kidd, LaCreis
    FASEB JOURNAL, 2015, 29
  • [4] Functions and mechanisms of miR-186 in human cancer
    Wang, Zhen
    Sha, Huan-Huan
    Li, Hai-Jun
    BIOMEDICINE & PHARMACOTHERAPY, 2019, 119
  • [5] miR-186 inhibits cell proliferation in multiple myeloma by repressing Jagged1
    Liu, Zengyan
    Zhang, Guoqiang
    Yu, Wenzheng
    Gao, Na
    Peng, Jun
    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2016, 469 (03) : 692 - 697
  • [6] miR-186 inhibits cell proliferation of prostate cancer by targeting GOLPH3
    Hua, Xing
    Xiao, Yu
    Pan, Wenhai
    Li, Meiyun
    Huang, Xiaoxiao
    Liao, Zexiao
    Xian, Qi
    Yu, Lina
    AMERICAN JOURNAL OF CANCER RESEARCH, 2016, 6 (08): : 1650 - 1660
  • [7] MIR-520f Regulated Itch Expression and Promoted Cell Proliferation in Human Melanoma Cells
    Sun, Ming-xia
    An, Qun
    Chen, La-mei
    Guo, Ling
    DOSE-RESPONSE, 2020, 18 (02):
  • [8] miR-186 suppresses cell proliferation and anchorage-independence in a metastatic prostate cancer cell line
    Jones, Dominique Z.
    Schmidt, M. Lee
    Hobbing, Katharine R.
    Clark, Geoffrey
    Kidd, LaCreis R.
    FASEB JOURNAL, 2016, 30
  • [9] MiR-769 promoted cell proliferation in human melanoma by suppressing GSK3B expression
    Qiu, Hai-jiang
    Lu, Xiao-he
    Yang, Sha-sha
    Weng, Chen-yin
    Zhang, E-keng
    Chen, Fang-chao
    BIOMEDICINE & PHARMACOTHERAPY, 2016, 82 : 117 - 123
  • [10] miR-922 regulates CYLD expression and promotes the cell proliferation of human hepatocellular carcinoma
    Liu, Jianping
    Su, Zheng
    Zeng, Yunjie
    Zhang, Huayao
    Yang, Shanglin
    Liu, Gaojie
    ONCOLOGY REPORTS, 2017, 37 (03) : 1445 - 1450